Pancreatic ductal adenocarcinoma (PDAC) is the most malignant digestive tumor and is characterized by late detection, early metastasis, and poor prognosis, with a 5-year survival rate of less than 7%. Although severe interstitial fibrosis and lack of blood supply are important features of PDAC tissue, the tumor cells are often accompanied by intense neovascularization. Many cytokines play important roles in promoting tumor angiogenesis directly or indirectly through the bridge of the pancreatic stellate cells (PSCs), but thein specific action mechanism is not entirely clear. Meanwhile, experimental results also showed that the expression of vascular endothelial growth factor (VEGF) was positively correlated with the secretion of galectin-1 and hepatocyte growth factor (HGF) from activated PSCs. Tumor angiogenesis is one of the characteristics of tumors, and angiogenesis is essential for the continuous growth, invasion, and metastasis of PDAC. However, there are relatively few studies on PDAC angiogenesis. Here, the authors address the effects of PSCs in the PDAC microenvironment on tumor angiogenesis, and the potential cancer treatment strategies targeting PSCs to block their function are also discussed.